Functional inactivation of menin, encoded by the MEN1 gene, causes the inherited multiple endocrine neoplasia type 1 (MEN1) syndrome and some but not all sporadic pancreatic endocrine tumors. Therefore, unraveling molecular events upstream or downstream of menin could point to other causative genes and/or regulatory events responsible for such tumor types. Proper tissue differentiation is dependent upon a precise control over the coordination between cell cycle events and the expression and activity of tissue specifying factors. This type of coordination could go awry to result in tumor formation. Our current efforts are directed towards studying 2 categories of genes for menin-regulated transcriptional, post-transcriptional, protein:protein interaction, and sub-cellular localization events: 1) Cyclin-dependent kinases and their inhibitors, and 2) Endocrine pancreas differentiation factors.